DM pt 2

Question 1

You diagnosed diabetes. You should now be asking what questions?

Answer 1

1) Is this type I or type II?
2) Are there signs of end-organ insensitivity to insulin?
3) Do family history, lifestyle, risk factors clue me into which type it is?

Question 2

Type 1 vs type 2: List and describe the sensitivity/ specificity of 4 types of autoimmune testing

Answer 2

1) Islet cell antibodies
-Sensitivity 44-100%
-Specificity 96%
2) Glutamic acid decarboxylase (GAD65)
-Sensitivity 70-90%
-Specificity 99%
3) Insulin autoimmune antibodies (IAA)
-Sensitivity 40-70%
-Specificity 99%
4) Tyrosine phosphatase
-Sensitivity 50-70%
-Specificity 99%

Question 3

True or false: The patient is going to help you to manage their care, in fact, they are the “primary care provider” of this pervasive illness

Answer 3

True

Question 4

What do you need to explain to newly diagnosed DM pts?

Answer 4

1) The nature of diabetes
The potential acute and chronic hazards they are going to face
2) Self-monitoring of blood glucose (especially if they require insulin)
3) Those on insulin will also need to be trained on basal and bolus insulin
-What’s the appropriate basal dose?
-How do they adjust their rapid acting for the carbohydrate content of their meals?
-Teach them to inject their medicine
4) Families and close friends or additional care-givers need to be educated on the signs of hypoglycemia
5) They need education on follow up with ophthalmology, foot and dental care
6) And, of course, they need to learn about diet and exercise

Question 5

The Diabetes Control and Complications Trial(DCCT):
1) What is it?
2) What did it establish?

Answer 5

1) Long term therapeutic study for type I pts
2) Established that “near” normalization of blood glucose in type I diabetics resulted in a delay in the onset and major slowing of the progression of vascular and neuropathic complications

Question 6

The Diabetes Control and Complications Trial (DCCT): What were the HbA1cs of the 2 arms of the study?

Answer 6

1) Intensive treatment group: mean HbA1c of 7.2%
2) Conventionally treated group: HBA1c averaged 8.9%

Question 7

The Diabetes Control and Complications Trial (DCCT):
1) Intensive Tx group had approximately 60% reduction in the risk of what 3 things compared with the conventional group?
2) Intensive group did have more weight gain and higher incidence of ___________

Answer 7

1) diabetic retinopathy, nephropathy, and neuropathy
2) hypoglycemia

Question 8

The Diabetes Control and Complications Trial(DCCT):
1) ADA recommends intensive insulin therapy in pts with type I DM after what age?
2) What are the exceptions?

Answer 8

1) Age of puberty
2) Those with advance CKD and older adults, since the risk of hypoglycemia outweighs benefit

Question 9

The UK Prospective Diabetes Study (UKPDS): What is it?

Answer 9

Multicenter study aimed at determining whether risk of macrovascular or microvascular complications could be reduced by intensive blood glucose control in type II pts.
-Documented a total of 27,000 patient years of intensive therapy

Question 10

The UK Prospective Diabetes Study (UKPDS): What treatment(s) did it use?

Answer 10

Used oral agents or insulin: metformin, sulfonylureas, or combination of the two, or insulin

Question 11

The UK Prospective Diabetes Study (UKPDS): What were the HbA1cs of the 2 arms of the study?

Answer 11

Intensive group: mean HbA1c levels of 7%
Conventional therapy: mean HbA1c levels of7.9%

Question 12

1) Findings supported that the intensive group showed benefit in what?
2) Showed that intensive therapy (which was demonstrated effective in DCCT trial) can be extended to _______________ patients

Answer 12

1) 25% reduction in microvascular disease as comparted to control
2) type II DM

Question 13

The UK Prospective Diabetes Study (UKPDS):
1) Showed that there is benefit to lowering HbA1c below ___%
2) There was _______ & there were higher rates of hypoglycemia in the intensively controlled group

Answer 13

1) 8.0%
2) wt. gain

Question 14

The UK Prospective Diabetes Study (UKPDS):
1) An additional feature of this study was the analysis of what?
2) What were the results of this?

Answer 14

1) BP regulation
2) Showed that tighter control of BP (median value 144/82 vs mean of 154/87) substantially reduced risk of microvascular disease and stroke (But not MI)
-In fact, BP control appeared to have more of an effect than did glucose control

Question 15

What are the targeted A1c goals for Patients with CKD?

Answer 15

1) Glycemic targets in CKD are the same as those without it
2) However, A1C (and even Fructosamine) may not be accurate in ESKD, so rely more on at home glucose measurements

Question 16

Type 1 Tx: What 2 basic things do they need?

Answer 16

These patients need a method of monitoring, if not by finger stick, then by continuous monitoring device
They will be on insulin

Question 17

T1DM: Describe the daily dose of insulin

Answer 17

Daily dose of insulin
0.5 units/kg/day
Half of this is the basal dose
The other half is divided over three mealtime doses

Question 18

1) Mealtime doses get tweaked by the carb to insulin ratio; define this ratio
2) How do you calculate this?

Answer 18

1) This is how many carbs one unit of insulin will eliminate when they eat and take their insulin
2) This number is 550 divided by the total daily dose of insulin
It will equal something like “15”
That means one unit of insulin eliminates 15 carbs on my plate
They will take this much insulin as their mealtime dose

Question 19

T1DM Tx: Describe correction factor

Answer 19

1) This is what they will take when their pre-meal blood sugar is higher than the goal you set
2) That goal might be something like 150, 120
-You will decide
3) This number is found by dividing 1650 by their total daily insulin dose
-They will also take this insulin at mealtime if it’s needed

Question 20

Insulin dosing for T1DM- Basal insulin:
1) What are the 2 options?
2) How is it calculated?

Answer 20

1) Insulin glargine or degludec once daily
(detemir often has to be dosed BID because of its short half life)
2) This number is (0.5 x kg) / 2 = “X”

Question 21

Describe how to calculate Insulin to carb dose based on the meal

Answer 21

This is the total carbs on the plate divided by their specific number (It’s probably about 15)
So, say they’re eating 50 carbs / 15 = about 3

Question 22

Correction factor for T1DM:
1) When is it needed?
2) Give an example using a goal of 120 and their glucose reads 170

Answer 22

1) They’ll need this if their pre-prandial glucose reading is high
2) They’ll need some additional insulin to bring that down
Most people with a carb ratio of 15 have a correction factor of about 50
So, they’ll be taking an extra unit of insulin to knock out those 50 extra points

Question 23

For dosing insulin at a meal, when exactly should they take it?

Answer 23

Tell them to take the insulin with their “first bite”

Question 24

1) The “___________phenomenon” describes a period of decreased insulin sensitivity between the hours of 3am and 8am
2) Patients on ____________________ will already be compensated by their hardware (something like 0.1 units per hour extra)

Answer 24

1) dawn
2) continuous monitoring pumps

Question 25

1) Explain the The Somogyi effect 2) When should readings be taken? 3) How is it managed?

Answer 25

1) occurs when nocturnal hypoglycemia leads to a compensatory hyperglycemia in the morning 2) Your patients will need to obtain readings during these hours At 3 am and 7am If you are finding low sugars in this window, take the following measures 3) Lower the nighttime basal dose OR, have the patient eat a snack at bedtime

Question 26

Describe how to deal with being sick with T1DM

Answer 26

Type I patients should avoid mealtime doses until they are eating solid food Continue basal insulin, and only dose correction factor If BG gets above 300, check urine ketones If present, seek immediate medical attention

Question 27

T2 DM: List and describe the following therapeutic considerations: 1) Cardiovascular and renal effects 2) Efficacy 3) Hypoglycemic risk

Answer 27

1) Metformin, liraglutide, semaglutide, empagliflozin and canagliflozin have known cardiovascular benefits SGLT2 inhibitors reduce risk of ESKD 2) DPP-4 inhibitors are of moderate efficacy All other agents of high efficacy 3) Sulfonylureas and insulins have increased risk

Question 28

T2 DM: List and describe the following therapeutic considerations: 1) Effect on weight 2) Cost

Answer 28

1) Metformin and DPP-4 are weight neutral GLP-1 and SGLT2 promote weight loss Sulfonylureas, insulins, (and to a lesser degree pioglitazone) are associated with weight gain 2) All but metformin and sulfonylureas are expensive Insulins can get expensive if you include the monitoring

Question 29

T2 DM: List and describe the following therapeutic consideration: Major side effects (not sure if we need to know)

Answer 29

Metformin: lactic acidosis, AKI. Discontinue if Cr > 1.7 or GRR < 30 Glitazones: fluid retention, fracture risk, macular edema, possible bladder cancer, don’t use in heart failure (NY class III or IV) GLP-1: N/V, pancreatitis DPP-4: possible pancreatitis SGLT2: UTI, genital mycotic infections, dehydration, cannot use if eGFR < 30 Sulfonylureas: check to see if there is renal dosing or contraindication in liver failure

Question 30

T2DM: Most of the time they still make some insulin For this reason, they may just wind up on what? Explain

Answer 30

Basal dosing: This could be something like 10 units daily OR you can give them 0.2 units / kg In either case, titrate to effect No more than 10% change at a time

Question 31

If you need to take full insulin regimen with basal and bolus, how do you do this?

Answer 31

use what you already know for type I

Question 32

At the time of diagnosis of Type I DM, there often remains significant beta cell function. This leads to what?

Answer 32

A brief clinical remission of the illness known as the “honeymoon phase”

Question 33

1) ___________________ is approved for pts 8 yo and up at high risk for type I DM -Must have impaired glucose tolerance and two positive antibodies 2) ___________ has also been tried

Answer 33

1) Teplizumab mzwv 2) Infliximab

Question 34

Intervention with low-fat diet and 150 minutes of moderate exercise per week slowed progression to T2DM by _____%

Answer 34

71%

Question 35

Metformin 850mg BID reduced risk by 31%, but is not effective in who?

Answer 35

Not effective in those with minimal obesity Not effective in the oldest age group

Question 36

Diabetic Retinopathy: After 20 years, 60% of ___________and virtually all of pts with _________ will have this

Answer 36

type II; type I

Question 37

Describe: 1) Diabetic cataracts 2) Diabetic retinopathy

Answer 37

1) Occur prematurely & correlate with the duration of DM and severity of hyperglycemia 2) After 20 years, 60% of type II and virtually all of pts with type I will have this a) Comes in two types: Non-proliferative & Proliferative

Question 38

Non-proliferative diabetic retinopathy: Define this and describe the 3 types

Answer 38

1) Microvascular changes are limited to the retina Can be mild, moderate, or severe 2) Mild: no vision loss When reduction of vision occurs, it is due to diabetic macular edema (focal or diffuse) or due to macular ischemia Severe: having one or more of the following Severe intraretinal hemorrhage and microaneurysms in 4 quadrants, venous beading in two or more quadrants, intraretinal microvascular abnormalities in at least one

Question 39

Describe Proliferative retinopathy

Answer 39

1) Neovascularization arising from optic disc or retinal vascular arcades -Prior to formation of new capillaries, ischemia often occurs, manifesting as cotton wool spots 2) Vision is usually normal until macular, edema, vitreous hemorrhage, or retinal detachment occurs 3) Proliferation into vitreous of blood vessels, with fibrosis, leads to vitreous hemorrhage or retinal detachment (this retinopathy has been known to worsen after bariatric surgery, or to continue when hyperglycemia is brought under tight control)

Question 40

DM ocular complications: 1) Tx? 2) F/u?

Answer 40

1) Optimizing blood glucose, BP, kidney function and serum lipids 2) Initially, patients should receive ophthalmologic exam every 3-4 months, then annually Avoid tobacco

Question 41

Diabetic Nephropathy: 1) Pathogenesis? 2) How to Dx?

Answer 41

1) -Microvascular damage; initially manifested by albuminuria -Then as kidney function declines, urea and creatinine rise 2) Albumin/creatinine ratio in early morning spot urine collected upon waking -Ratio greater than 30 mcg/mg suggests abnormal microalbuminuria -Should have at least two positives over a three-to-six-month period

Question 42

Diabetic Nephropathy: How do you Tx?

Answer 42

1) Glycemic control as well can reduce hyperfiltration and elevated microalbuminuria 2) Antihypertensive therapy: ACE inhibitors -An ACE inhibitor in normotensive pts with DM impedes progression to proteinuria and prevents increase in albumin excretion rate 3) Pts progressing to kidney disease are given SGLT2 therapy

Question 43

Peripheral Neuropathy: Describe the pathogenesis

Answer 43

1) MC form 2) Stocking-glove pattern, due to length of neuron (long one’s are more susceptible) 3) Impairs both motor and sensory Sensory impaired first: dulled perception of vibration, pain, and temperature > leading to sometimes severe burning pain

Question 44

Peripheral Neuropathy 1) Dx? 2) Tx & f/u?

Answer 44

1) Examine with filament -Those who cannot feel it, are at risk for unperceived injury 2) Diabetic foot exam, repeat screening -Aggressive treatment of injury and involvement of wound care when necessary -Neuropathic pain can be treated with tricyclic antidepressants, or with gabapentin

Question 45

Charcot foot: 1) Explain the pathogenesis 2) What will the pt experience?

Answer 45

1) Denervation of small muscles of the foot can result in clawing of the toes and displacement of the sub metatarsal fat pad anteriorly -This in combination with Charcot arthropathy 2) Pain and swelling -IF untreated “rocker bottom” deformity

Question 46

Diabetic neuropathic cachexia: 1) What is this? 2) How is it treated?

Answer 46

1) Syndrome of symmetric peripheral neuropathy, profound weight loss (up to 60% of total body weight), panful dysesthesias affecting proximal lower limbs, hands and trunk 2) Insulin and analgesics – prognosis is good

Question 47

Autonomic Neuropathy: GI system: 1) Describe Pt/Dx 2) What are the 2 main medications to Tx?

Answer 47

1) N/V postprandial fullness, reflux, dysphagia (constipation, diarrhea, or both) -Gastroparesis -Unexpected fluctuations and variability in BG after meals 2) Gastroparesis is treated with metoclopramide You can also try erythromycin

Question 48

Autonomic Neuropathy: GU: How do you Tx?

Answer 48

1) Incomplete bladder functioning: bethanechol can sometimes help 2) Erectile dysfunction: PDE5 inhibitors 3) Orthostatic hypotension: fitted stockings, tilting head of bed, rising slowly, sometimes fludrocortisone can be considered (but watch for supine hypertension and potassium derangement)

Question 49

Heart disease: 1) Pathogenesis? 2) Effect on pt?

Answer 49

1) Atherosclerosis MC, second is microangiopathy of the heart In type II this results from: hyperglycemia, hyperlipidemia, abnormalities of platelet adhesiveness, coagulation factors, HTN, oxidative stress and inflammation 2) 3-5 times more likely to have MI

Question 50

Heart disease: 1) Dx? 2) Tx?

Answer 50

1) CT chest, lipids, angiogram all investigate CAD 2) Lower LDL -ASA -In those with hx of stroke or MI, use for secondary prevention -In those with no such hx but who are at high risk, and who are low bleeding risk (Not for those over 70)

Question 51

Peripheral vascular disease 1) Pathogenesis? 2) Pt Sx?

Answer 51

1) Atherosclerotic plaque > turbulent flow > intimal damage 2) Ischemia of the lower extremities, ED, intestinal angina Gangrene of the feet is 30x greater Made worse by concomitant neuropathy

Question 52

Peripheral vascular disease Tx?

Answer 52

Prevent foot injury! Avoid tobacco Control BP, Lower cholesterol

Question 53

Skin and Mucous Membrane Complications: 1) Path? 2) Pt Sx? 3) Tx?

Answer 53

1) chronic pyogenic infection, candidal infection 2) Chronic, non-healing ulcers of lower extremities Candidal infection in axillae, below the breasts, between the fingers, vulvovaginitis 3) Antibiotic vs. antifungal

Question 54

Emergent conditions: Describe DKA Sx

Answer 54

Weakness Kussmaul breathing Tachycardia N/V Generalized abdominal pain Polyurea/polydipsia Dry mucous membranes Fruity breath (can become altered)

Question 55

Emergent conditions: Describe HHS Sx

Answer 55

Altered mental status Weakness Polyurea/polydipsia Dry mucous membranes

Question 56

What are the lab values for DKA?

Answer 56

Hyperglycemia > 250 Metabolic acidosis with blood pH < 7.3 Serum positive for ketones Widened anion gap.

Question 57

What are the lab values for HHS?

Answer 57

Hyperglycemia > 600 Serum osm > 310 No acidosis: pH > 7.3 Serum bicarb > 15 Normal anion gap

Question 58

How do you Tx DKA?

Answer 58

1) Fluid resuscitation 2) Potassium monitoring 3) Insulin drip 4) Look for the inciting cause 5) ICU admission

Question 59

How do you Tx HHS?

Answer 59

(Same Tx as DKA) 1) Fluid replacement 2) Potassium monitoring 3) Insulin drip 4) Look for the inciting cause 5) ICU admission

Question 60

True or false: The Tx for DKA and HHS is the same

Answer 60

True